A NIMA-related protein kinase suppresses ectopic outgrowth of epidermal cells through its kinase activity and the association with microtubules
A NIMA-related protein kinase suppresses ectopic outgrowth of epidermal cells through its kinase activity and the association with microtubules
复制标题
DOI：
10.1111/j.1365-313x.2008.03445.x
复制
发表时间：
2008-06-01
期刊：
影响因子：
7.2
通讯作者：
Watanabe, Yuichiro
中科院分区：
文献类型：
--
作者：
Motose, Hiroyasu;Tominaga, Rumi;Watanabe, Yuichiro
为了研究细胞形态发生的遗传，我们分离出拟南芥的功能丧失突变体，命名为ibo 1。ibo 1突变导致下胚轴和叶柄表皮细胞中间的局部生长，从而形成突起。在拟南芥中，下胚轴表皮通过涉及透明种皮GLABRA 1（TTG 1）和GLABRA 2（GL 2）的机制分化成两个交替的细胞群，即气孔细胞群和非气孔细胞群。ibo 1突变体的异位突起优先在表达GL 2的非气孔细胞文件中诱导。TTG 1依赖性表皮图案化是ibo 1中突起形成所必需的，这表明IBO 1在表皮细胞特化的下游起作用。药理学和遗传学分析表明，乙烯促进IBO 1突起的形成，这意味着IBO 1的作用拮抗乙烯抑制径向生长。IBO 1与NEK 6相同，NEK 6编码一种Never In MitosisA（NIMA）相关蛋白激酶（Nek），其序列与真菌、藻类和动物中参与微管组织的Nek相似。ibo 1 -1突变，其中激活环中的保守Glu残基被Arg取代，完全消除其激酶活性。GFP标记的NEK 6的细胞内定位显示，NEK 6主要积累在与皮质微管和与γ-微管蛋白复合物的推定组分相关的细胞质点中。NEK 6的定位由C-末端结构域调节，该结构域在ibo 1 -2等位基因中被截短。这些结果表明，NEK 6在细胞形态发生的控制中的作用依赖于其激酶作用和与皮质微管的关联。
To study cellular morphogenesis genetically, we isolated loss-of-function mutants of Arabidopsis thaliana, designated ibo1. The ibo1 mutations cause local outgrowth in the middle of epidermal cells of the hypocotyls and petioles, resulting in the formation of a protuberance. In Arabidopsis, the hypocotyl epidermis differentiates into two alternate cell files, the stoma cell file and the non-stoma cell file, by a mechanism involving TRANSPARENT TESTA GLABRA1 (TTG1) and GLABRA2 (GL2). The ectopic protuberances of the ibo1 mutants were preferentially induced in the non-stoma cell files, which express GL2. TTG1-dependent epidermal patterning is required for protuberance formation in ibo1, suggesting that IBO1 functions downstream from epidermal cell specification. Pharmacological and genetic analyses demonstrated that ethylene promotes protuberance formation in ibo1, implying that IBO1 acts antagonistically to ethylene to suppress radial outgrowth. IBO1 is identical to NEK6, which encodes a Never In Mitosis A (NIMA)-related protein kinase (Nek) with sequence similarity to Neks involved in microtubule organization in fungi, algae, and animals. The ibo1-1 mutation, in which a conserved Glu residue in the activation loop is substituted by Arg, completely abolishes its kinase activity. The intracellular localization of GFP-tagged NEK6 showed that NEK6 mainly accumulates in cytoplasmic spots associated with cortical microtubules and with a putative component of the gamma-tubulin complex. The localization of NEK6 is regulated by the C-terminal domain, which is truncated in the ibo1-2 allele. These results suggest that the role of NEK6 in the control of cellular morphogenesis is dependent on its kinase action and association with the cortical microtubules.